51 - Charcot Reconstruction Flashcards
Deep thoughts with old man Greenhagen
- “In the last analysis, we see only what we are ready to see, what we have been taught to see. We eliminate and ignore everything that is not a part of our prejudices” Jean Martin Charcot
Charcot neuropathy
- Non-infectious destruction of bone associated with neuropathy
- Initial recognition can be difficult
- Can be devastating
- Now common in diabetics with neuropathy
A little history…
- Sir William Musgrave
o First to describe neuropathic joint 1703, called it “neuropathic arthritis” and noted that it was a complication of venereal disease (VD) - John Kearsley Mitchell
o Suggested a relationship between a spinal cord lesion(TB caries of the spine) and arthropathy of the foot and ankle, referenced by Charcot in his first papers - Silas Weir Mitchell
o Gunshot wounds during Civil War, nutrition of joints, spinal injury leads to rheumatic sx - Jean-Martin Charcot
o 1825-1893, one of most celebrated French physicians, transformed Salpetriere into world renowned institution
o Arthropathy associated with progressive locomotor ataxia (tabes dorsalis)
o Early findings published in 1868, referenced Mitchell and Mitchell - Virchow and Volkmann
- William Reily Jordan
Pathophysiology
Pathophysiology
- 7th International Medical Congress – London, August 2-9, 1881
- “A gathering the like of which has never been witnessed before, and in all probability will never be paralleled in our day.” The Lancet
Historical prospective
- 1936: Pathology linked to diabetes by WR Jordan
- 1955: Miller and Lichtman established the increasing frequency in diabetic patients
- 1966: Eichenholtz classified deformity based on radiographic progression KNOW THIS
French theory = “Neurotrophic” theory
- Central nervous system degeneration caused a neurogenic deficit in bone nutrition
- Known causes of neuropathic arthropathy at the time generally related to central injuries
- No trophic factors identified to support this theory
German theory = “Neurotraumatic” theory
- Loss of protective sensation allows for repetitive microtrauma in the insensate limb
- Normal fracture healing does not occur
- Volkman and Virchow argued that neuroarthropathy was merely “traumatic arthritis”
- Fails to explain development in paralyzed patients unable to ambulate
Neurovascular theory – TODAY’S THEORY
- Increased blood flow in region of destruction – they’re bright red, so we know there is blood
- Sympathetic failure causes a hyper-vascular reflex and a state of overactive bone resorption
- Bone scans show increased uptake in Charcot arthropathy
- Due to sympathetic denervation or local inflammatory process?
The common denominator of disorders which cause neuropathic arthropathy is:
“The absence or decrease in pain sensation in the presence of uninterrupted physical activity” o Tabes dorsalis or syringomyelia o Congenital insensitivity to pain o Spinal Cord Injury or peripheral Nerve Inj. o Idiopathic neuropathy o Diabetes o Leprosy o Myelomenigocele or Spina Bifida o Chronic Alcoholism o Transplant patients or chemotherapy
REMEMBER: Charcot is…
REMEMBER: Charcot is NEURO-ARTHROPATHY ***
Unifying theory
- Best understanding of the etiology of neuropathic arthropathy at this point is multifactorial
- Balance between RANKL (receptor activator of nuclear factor kappa beta ligand) and osteoprotegerin (OPG)
- RANKL activates RANK, osteoclasts, etc. in order to cause bone destruction
- OPG has opposite effect – it stops RANKL form binding and therefore prevents osteoclasts from becoming activated and resorbing bone
- Vascular calcification in DM occurs by same pathway (intima-MEDIA-adventitia) – If you see vascular calcification, be suspicious
RANKL/OPG signaling pathology
- RANKL binds to RANK, inducing a signaling cascade leading to differentiation of osteoclast precursor cells and stimulating the activity of mature osteoclasts
- Functions as a decoy receptor for RANKL, and is thus an inhibitor of osteoclastogenesis
Amount of bone resorption depends on the balance of RANKL and OPG
- If RANKL and OPG are present in equal amounts, bone is maintaining itself
- If RANKL is at a higher concentration, more bone resorption occurs
- If OPG is at a higher concentration, less bone resorption occurs
BMD and patterns of Charcot’s Arthropathy
- Patient suffering from Charcot have altered bone mineral density (BMD)
- Herbst et al, 2004 showed that patients with normal BMD tend to have dislocations due to trauma and patients with diminished BMD tend to have fractures due to trauma
- Greenhagen et al, 2011 showed that BMD does not seem to recover after a Charcot event
Typical patient
- 55-60 yrs. old (mean 57), mean years as a diabetic is 15 yrs. w/ 80% having it for at least 10 yrs.
- Prevalence varies with ranges from 0.03% to 7.5%, so a good ballpark number is 1%
- **Bilateral involvement in 9-35% ** because when you treat one side, it typically involves off-loading, leading to overuse to the other side and eventually Charcot
- The longer you have diabetes, the worse your Charcot because the worse your neuropathy
- A diabetic with neuropathy is classified as a “complicated diabetic”
Epidemiology
- Sinha, et al, in one of the first large studies on diabetics with Charcot, reported that 1 in 680 diabetics had Charcot (n = 68,000)
- 10 year Danish study (n = 4000) found an annual incidence of initial Charcot attack of 0.3%
- Lavery et al, 2003 (n = 1666 diabetics) found a much higher in US (11-6%)
- True prevalence unknown – could be as high as 25% when considering wrong diagnoses
Diagnosis of Charcot - Three aspects to consider
o History
o Physical Exam
o Radiographic Interpretation
Diagnosis history
- Hot, Swollen Foot
- +/- Trauma
- Just because they don’t remember trauma doesn’t mean they didn’t have it – 55-75% do not remember any trauma
- Trauma is not limited to sprains and strain – Joint infections and surgical trauma can induce this
- Mild/ moderate pain (if you can’t feel anything but you can feel pain – WARNING SIGN)
- No previous ulcerations and no systemic signs of infection
Diagnosis physical exam
- Swollen, (deformed?) Foot
- Warmth
- Erythema
- Joint effusion
- Neuropathy
- +/- Ulcerations
- Contralateral foot
- Elevation test – with inflammation/venous stasis, patient will demonstrate dependent rubor with elevation pallor
Typical acute presentation
- So, the typical acute presentation of a Charcot foot is a red, hot, swollen foot
- Typically this is painless or only mildly painful unilateral swelling of extremity
- The Acute presentation can mimic cellulitis, gout, osteomyelitis and even DVT
- Plain films may appear normal initially
- Physical exam may reveal joint laxity w/ crepitus, decreased DTRs, vibration, and proprioception
- Patient may have bounding pulses, calor, rubor, tumor, anhidrosis +/- xerosis, cutaneous ulcer
- In the chronic Charcot you may see a Rocker bottom foot with plantar ulcerations
Natural history
- Advanced Glycosylation (pull of triceps, intrinsic atrophy, alters mechanical bone properties)
- Midfoot Collapses and Reversal of Arch (“rockerbottom” deformity)
- Tarsal prominence leads to Increased Plantar Pressure
Diagnosis – X-ray
- EARLIEST sign is bone resorption and soft tissue swelling, before architecture is altered
- Bony destruction, Fracture, Subluxation and Dislocation may also occur
- No wound = no osteo (hematogenous osteo is typically in kids due to high blood turbulence at growth plates, so unless there is or has been an open wound, it’s not osteo)
Brodsky Anatomic Classification
Really important because the majority of research is ortho
- Type 1
- Type 2
- Type 3a/3b
Brodsky Anatomic Classification - Type 1
o Tarsometarsal and naviculocuneiform jts - MIDFOOT
o MOST COMMON (60%) and most stable
Brodsky Anatomic Classification - Type 2
o Transverse tarsal and subtalar joints
o Second most common (35 %)
o Hindfoot instability leading to ulceration, typically over the talar head
Brodsky Anatomic Classification - Type 3a/3b
3a = ankle 3b = calcaneus
o 5% of Charcot but MOST UNSTABLE
o Frequently requires surgery, high risk of major amputation (BKA, AKA)
o VERY UNSTABLE
Sanders and Frykberg Classification
Main difference is “Pattern I” which focuses on forefoot Charcot
- Pattern I
- Pattern II
- Pattern III
- Pattern IV
- Pattern V
Sanders and Frykberg Classification - Pattern I
Pattern I: Forefoot (15%)
o IPJs and phalanges
o MPJs and metatarsals
Sanders and Frykberg Classification - Pattern II
Pattern II: Tarsometatarsal joints (40%)
o LisFranc’s or tarsometatarsal joints
Sanders and Frykberg Classification - Pattern III
Pattern III: Proximal midfoot (30%)
o Naviculocuneiform, talonavicular and calcaneocuboid joints
Sanders and Frykberg Classification - Pattern IV
Pattern IV: Ankle and subtalar joints (10%)
o Ankle joint, subtalar joint
Sanders and Frykberg Classification - Pattern V
Pattern V: Rearfoot (5%)
o Calcaneus = rare
** Eichenholtz Classification ** REALLY IMPROTANT – NEED TO KNOW
General
o This classification system is important because it helps to guide treatment
o Includes 3 stages which incorporate both radiographic and clinical findings
Stages
- Stage I
- Stage II
- Stage III
** Eichenholtz Classification - Stage I
Stage I: developmental
o Red, hot, swollen joint (+/- pain)
o Radiographically, bones look enlarged (“blown up”)
** Eichenholtz Classification - Stage II
Stage II: coalescence
o No longer red, hot and swollen – clinical symptoms begin to regress
o Bones are not continuing to destroy themselves, they are starting to calm down
o We see the bones begin to coalesce radiographically
** Eichenholtz Classification - Stage III
Stage III: consolidation
o The bones become “the rock” and harden
o Continues on for a long period of time, but it is a cycle, so will go back to stage I
**Stage 0 Charcot in situ - KNOW THIS ** (“if you gain one thing from today, this is it”)
- ** ANY neuropathic patient who has a traumatic injury is a stage 0 Charcot **
- Period of inflammation after acute trauma in a patient with neuropathy
- Most important stage to recognize because no deformity has occurred yet and we can prevent the progression into Charcot
- We can arrest the process and prevent Stage 1 from occurring, so always be vigilant
Wukich et al, 2001
- Studied patients with undetected early Charcot neuropathy
- Group I: patients who did NOT progress to active Charcot
- Group II: patients who DID progress to active Charcot
- They found that the longer you wait to make the correct diagnosis of early Charcot neuropathy, the more complications occur
Treatment
- “If you do not have a proven treatment for certain illnesses, bid your time, do what you can, but do not harm your patients.” Jean Martin Charcot
Goals of treatment
- Plantigrade, stable, shoeable/braceable foot
- Heal any ulcers and prevent recurrences
- Decrease or eliminate pain
- Avoid amputation and maintain ambulation
Management is based on…
- Acuteness of symptoms
- Anatomic Pattern
- Degree of involvement (Deformity, Instability, Fractures, Fragmentation)
- Presence of Ulcer /Infection
Non-surgical management – Stage 0 and 1
- Remember stage 0 or 1 means they are either already red/hot/swollen or they might progress
- Patient education = MOST IMPORTANT
-
Immobilization
o Total contact Casting & Non-WB
o Nonweight bearing
o Instant TCC
Total contact cast
- Stage 1 Charcot
o inzur et al 2006
o All progressed to uneventful consolidation and “healing” of their acute symptoms
o All were independent community ambulators
o Subjects’ feet were deemed sufficiently “stable” for therapeutic prescription footwear at an average of 9.2 (range 6 to 16) weeks - Still “gold standard” but he never does it
Bisphosphonates
- Potent inhibitors of osteoclastic activity
- IV pamidronate - single infusion 90 mg
- “Pamidronate given as a single dose leads to a reduction in bone turnover, symptoms and disease activity in diabetic patients with active Charcot neuroarthropathy.”
- Problems with this drug
Non-surgical management
Long term bracing (once they’ve moved on to stage 2)
o Custom inserts/shoes
o Double upright brace
o Patella Tendon Bearing Orthosis (PTB)
o CROW = Charcot Restraint Orthotic Walker
How effective is nonoperative treatment in Charcot patients? KNOW THIS
- **60% ** (reports vary from 50-90% successful)
- Pinzur, 2004 showed that we are able to manage 60% of midfoot Charcot without surgery at minimum of 1 year follow up
- We do not know how effective treatment is for the ankle, hindfoot or transverse tarsal joints
Which patients need surgery?
- Deformities causing pain, instability or an inability to brace a deformity
- Impending compromise of the skin, non-healing ulcers or recurrent ulcers due to malalignment
- 25-50% of patients will require some type of surgery
Signs of failure
- Lateral talar-first metatarsal angle (Meary’s angle) greater than 27 degrees
- This means ulceration is impending***
Risk of amputation
- No ulcer @ presentation – 7% risk of amputation
- Ulcer @ presentation – 28% risk of amputation
- Recurring (2 or more) ulcers after treatment for Charcot – 31% risk of amputation
Surgical treatment
- Two basic boney principles – Exostectomy (remove it) and arthrodesis (fuse it)
- Don’t forget your soft tissue balancing
- Limb salvage procedure – No clear guidelines and numerous techniques
Lack of surgical EBM – THIS IS BAD
- Lowery et al, 2012, 430 articles cited from 1963-2008, 85 articles met the criteria for inclusion
- 981 patients, NO Level 1, 2 or 3 studies
- Four surgeons have reported on 54.2% of the patients cited over the past 45 years.
Surgical treatment: Exostectomy
- Used to prevent or cure plnatar ulceration
- Effective if midfoot deformity stable, but the concern is iatrogenic instability
- Patient may be WB
- Limited use in the central and lateral midfoot (because these are WB surfaces)
Surgical treatment: Midfoot reconstruction
- Midfoot arthrodesis (intractable ulceration or instability)
- Prolonged healing time to obtain union (3+month)
- Rigid fixation required
- External Fixation if a wound is present
Surgical treatment: Calcaneal reconstruction
- Calcaneal avulsions (Achilles pulls it off) or break fractures the most common forms
- Bone is very soft
- Consider fracture excision and tendon reattachment
- Screws alone will not work
Surgical Treatment: Ankle Reconstruction
- Ankle Charcot arthropathy
- Usually following ankle trauma leading to ulcer/pending ulcer or unstable ankle
- Prolonged healing time to obtain union (3+month)
- Rigid fixation required compression screws, blade plate, IM Nail
Steps for arthrodesis correction
- Surgical pre-planning
- K-wires as a guide for the osteotomy
- Remove corrective wedge
- Fusion site reduction
- Temporary stabilization
External fixation
- Excellent for wound healing and skin flaps
- Used in hybrid and staged therapies, allows tri-planar correction
- Wukich et al, 2008 showed high complication rates especially in DM patients
*****Superconstructs are defined as follows…
- Fusion extends beyond zone of injury to include joints that aren’t affected to improve fixation
- Bone resection performed to shorten the extremity to allow for adequate reduction of the deformity without undue tension on the soft tissue envelope
- Use of the strongest fixation device that can be tolerated by the soft tissue envelope
- Application of the fixation devices in a position that maximizes mechanical function
*****Types of superconstructs
- Plantar Plating
- Locking Plate Technology
- Axial Placed Screws
- Intramedullary fixation
- Hybrid fixation
Plantar plating
- Span area of Charcot involvement better quality bone
- Tension side placement
- Excess dissection and periosteal stripping (wound complications?)
Locking plate technology
- Fixed angle construct – Excellent choice for osteoporotic bone (break the apple example)
- An interlocking plate is like a strong family – when they work together they are stronger than the individual parts
Axial screw placement (“Beaming”)
- Solid or cannulated screws within medullary canal of bone (antegrade or retrograde)
- Sammarco, 1991 – Used in calcaneus to 4th metatarsal
- Screw placement helps reduction of deformity
- Fixation is perpendicular to joint for arthrodesis
- Eliminates stress risers, no exposed hardware, limited exposure
- Accepts tension dorsal/plantar
Intermedullary nails
- Allow axial load and can be dynamized to stimulate fusion site
- Nakul, 2011 showed that intermedullary screws are superior to external fixation
Hybrid fixation
- “Where we’re at today – a mixture of methods”
- Locking plates and beaming, internal and external fixation, AOFAS recommendation
- Double rule (always double fixation for Charcot patients)
Soft tissue balancing
- Role of the triceps surae – primary deforming force in Charcot
- TAL vs. Gastroc – Greenhagen et al, 2012 showed lower risks, but may still occur
- Laborde, 2016 showed it can prevent deformity progression and ulcer recurrence
Exostectomy EBM
- Useful for relieving pressure from bone that cannot be accommodated w/ prosthetics/orthotics
- Grade C Recommendation (treatment is supported by level IV studies)
Arthrodesis with realignment EBM
- Useful in patients with pain, instability or recurrent ulcers who fail non-operative treatment
- Grade C Recommendation (treatment is supported by consistent Level IV studies)
Achilles EBM
- Achilles tendon or gastrocnemius lengthening reduces forefoot pressure and improves the alignment of the ankle/hindfoot to the midfoot/forefoot and allows forefoot ulcers to heal
- Grade B Recommendation (treatment is supported by higher level studies)
Fixation EBM
- Inconclusive evidence to recommend one form of fixation over another ( i.e. internal vs. external) in patients who are not infected
- Grade I recommendation (studies are heterogeneous and not comparable)
** WHAT YOU NEED TO KNOW **
- What is the most common location for a Charcot event?
- What are the Eichenholtz stages and what is the most important stage to recognize?
- What are the primary non-operative treatments?
- What are the two primary treatments for Charcot bone deformities?
- What are the principles of superconstruct?
- What soft tissue procedures may be necessary?
